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Medical Science ONE and HALF SYNDROME – a CASE KEYWORDS : Medial Longitudinal Fasciculus, Pontine Infarct ,Internuclear REPORT Ophthalmoplegia

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Medical Science ONE and HALF SYNDROME – a CASE KEYWORDS : Medial Longitudinal Fasciculus, Pontine Infarct ,Internuclear REPORT Ophthalmoplegia Research Paper Volume : 4 | Issue : 1 | January 2015 • ISSN No 2277 - 8179 Medical Science ONE AND HALF SYNDROME – A CASE KEYWORDS : Medial longitudinal fasciculus, pontine infarct ,Internuclear REPORT ophthalmoplegia . * Dr. Sachinkumar Department of medicine , Govt Medical College, Miraj , District- Sangli, Maharashtra. patankar 416416. * Corresponding Author Dr. Rajendra V Bhagwat Research Scholar, Acharya Nagarjuna University, Guntur, A.P. Dr. P D Shingade Department of English, Acharya Nagarjuna University, Guntur, A.P. India Dr. Suraj Goyanka Department of English, Acharya Nagarjuna University, Guntur, A.P. India ABSTRACT We report a case of 29 year old female who presented with features of sudden onset ptosis of right eye with gait instability and diplopia. Clinical examination revealed ocular position of the right eye on forward gaze fixed at the midline, while the left eye was abducted. On rightward gaze, neither eye could pass the midline, and on leftward gaze the left eye was abducted with monocular nystagmus suggestive of internuclear ophthalmo- plegia. Introduction area of altered intensity on posterior aspect of pons sug- The one-and-a-half syndrome is a clinical disorder of ex- gestive of acute infarct. Patient was managed conservative- traocular movements characterized by a conjugate horizontal ly with anticoagulants with a regular check on her vitals in palsy in one direction plus an internuclear opthalmoplegia in view of the strategic location of infarct. Over the days, the the other. It is due to a unilateral lesion of the dorsal pontine patient became symptomatically better although oscillop- tegmentum, involving the ipsilateral paramedian reticular sia due to abducting nystagmus of her non-paretic left eye formation, internuclear fibers of the ipsilateral medial lon- still persisted. She is on regular neurology follow up and is gitudinal fasciculus and, usually, the abducens nucleus. The doing well. main causes of this rare syndrome are stroke and multiple sclerosis. Other causes include tumors, AV malformations, basilar artery aneurysms and rarely, vasculitis, brainstem tu- berculoma and neurocysticercosis. CASE REPORT- A 29-year-old female patient was admitted to our institution with sudden onset of drooping of right eyelid, vertiginous feeling, gait instability and diplopia. She denied any history of weakness of any part of the body, paresthesias or numb- ness of limbs or face, urinary incontinence, deafness, tinnitus or any slurring of speech. She volunteered that she experi- enced sudden onset drooping of her right eyelid with diplo- pia. She has no past history of being hypertensive or diabetic. On admission, she had Glasgow coma score of 15/15 and her blood pressure was 140/90 mmHg. Her pulse was regular and equal on both sides with all peripheral pulses present. The ocular position of the right eye on forward gaze was fixed at the midline, while the left eye was abducted. For horizontal ocular movements, only the left eye could abduct with mo- nocular horizontal nystagmus. Also, there was conjugate gaze palsy to right, indicating horizontal right one-and a-half syn- drome i.e. on rightward gaze, neither eye could pass the mid- line, and on leftward gaze, horizontal jerky nystagmus in the abducting left eye was noticed. Vertical and rotatory nystag- mus was absent. There was no diplopia in primary gaze but she experienced horizontal crossed diplopia in leftward gaze. Vertical eye movements were preserved. Visual acuity was 6/6 (Snel- len) and N/6 in both eyes. Pupillary reactions were normal. The fundi were normal with no evidence of papilledema. No other neurologic deficit was seen. Rest of the systemic examination was also inconclusive. Her main symptom at this time was oscillopsia due to the abducting nystagmus of her on-paretic right eye, which was only relieved with occlusion of the eye with a patch. A clinical diagnosis of one-and-a-half syndrome secondary to a cerebrovascular event was made. And MRI of the brain showed small focal IJSR - INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH 365 Research Paper Volume : 4 | Issue : 1 | January 2015 • ISSN No 2277 - 8179 by unilateral lesions in the brain above the level of the oculomo- tor nucleus may vary according to the size and location of the lesion.The abducens nucleus (AN): extensive experimental data from cats and monkeys(3 4) suggest that the AN contains two types of cells, i.e., motoneurons which innervate the ipsilateral external rectus muscle (magnocellular motor neurons) and ex- citatory internuclear neurons that decussate at the level of the nucleus, ascend in the contralateral MLF and terminate at the medial rectus subdivision of the oculomotor nuclear complex. The paramedian pontine reticular formation (PPRF): numerous experimental studies in monkeys have produced data supporting the importance of the PPRF for integration of horizontalconju- gate gaze (4,6 8 10). Smaller lesions (1 to 2 mm) in the tegmen- tum of the pons, specifically in the PPRF, induce paralysis of ipsi- lateral conjugate gaze for as long as one year. Outside the pons the amount of tissue destruction necessary to affect horizontal gaze is much greater than in PPRF lesions(10). The PPRF contains two main types of neurons associated with eye movements, the phasic and the tonic cells. The former (ex- citatory burst neurons) are active during saccades, namely all kinds of rapid eye movements (voluntary saccades and quick phases of nystagmus). DISCUSSION Intemuclear ophthalmoplegia (INO): the INO is characterized In 1967,Miller Fisher(9) described a syndrome,he termed “one- by paresis or paralysis of the ipsilateral eye adduction - on at- and-a-half-syndrome” (OAHS) consisting of a “conjugate lat- tempted horizontal gaze to the contralateral side - and horizon- eral gaze palsy in one direction, plus one half of a gaze palsy in tal jerk nystagmus in the contralateral abducting eye. Typically the other”. Many aetiologies of OAHS have been described(1,2) convergence is preserved if the lesion does not extend to the mostly vascular, but also demyelinating and neoplasic disorders. mesencephalon. Bilateral lesions cause bilateral defects in ad- The syndrome usually results from a single, unilateral and rela- duction and nystagmus in the abducting eye. In addition there tively small lesion at the dorsal tegmentum of the lower pons. are nystagmus on upward gaze, as well as bilateral partial pto- Occasionally an ocular paralysis occurs, one eye looking ahead sis. Lesions of the MLF do not cause paralysis of conjugate hori- without any horizontal movement and the other staying ab- zontal or vertical gaze(7). Upgaze palsy, downgaze palsy, com- ducted. The latter eye does not move beyond the midline when plete vertical gaze palsy and vertical saccade for both upward horizontal movements are tested. Vertical eye movements are and downward gaze have been known to be related to bilateral relatively preserved. In OAHS the abducens nucleus (AN) and/ lesions involving the rostral interstitial nucleus of medial longi- or the paramedian pontine reticular formation (PPRF) located tudinal fasciculus (RiMLF) cell group and the posterior commis- rostrally and ventrally to that nucleus are damaged, producing sure(5).Paralytic pontine exotropia (PPE): the presence of exotro- an ipsilateral conjugate gaze palsy. Damage to the ipsilateral me- pia in OAHS was first observed by Fisher(9) In the acute phase, dial longitudinal fasciculus (MLF), which lies at the same level the exotropic eye shows abduction nystagmus during attempts or just above the AN, accounts for the unilateral internuclear to move it further laterally, and there is extreme slowness of ad- ophthalmoplegia (INO).In addition, during the acute phase, exo- duction when the eye moved to the midline.Again, normal mid- tropia of the contralateral eye, no deviation, or less commonly, brain ocular motor functions are shown by intact vertical gaze, esotropia of the eye ipsilateral to the lesion secondary to the pa- convergence, and pupillary constrictor reflex activity. In conclu- resis of the sixth nerve, may be seen in primary position of gaze. sion, the semiological diagnosis of the OAHS is comparatively The present patient had a deficit of horizontal gaze to the right simple and allows great anatomical precision. Peripheral facial side combined with a paresis of palsy without gustatory deficit is a common associated sign and eventually the most exuberant symptom. adduction to the opposite direction. In this syndrome, the nor- mal vertical eye movements and convergence suggest that motor fibers and nuclei of the third cranial nerves were preserved. The degree and duration of the horizontal gaze impairment caused REFERENCE 1. André C, Castro ALZ, Vincent MB, Mattos JP, Maranhão-Filho PA, Novis SAP. Sindrome "one-and-a-half: considerações | anatomoclínicas a propósito de um caso. Arq Neuropsiquiatr 1989;47:365-370. | 2. Azevedo D Jr. Pontine tegmentum hematoma: a case report with the "one-and- a-half syndrome without pyramidal tract | deficit. Arq Neuropsiquiatr 1995;53:475-480. | 3. Baker R, Highstein SM. Physiological identification of interneurons and motoneurons in the abducens nucleus. Brain Res | 1975;91:292-298. | 4. Bender MB. Brain control of conjugate horizontal and vertical eye movements: a survey of the structural and functional | cor- relates. Brain 1980;103:23-69. | 5. Bogousslavsky J, Meienberg O. Eye-movement disorders in brain-stem and cerebellar stroke. Arch Neurol 1987;44:141-148. | 6. Büttner U, Fuhry L. Eye movements. Curr Opin Neurol 1995;8:77-82. | | | | | | | | | 7. Christoff N, Anderson PJ, Nathanson M, Bender MB. Problems in anatomic analysis of lesions of the median longitudinal | fasciculus. Arch Neurol 1960;2:293-304. | 8. Cohen B, Komatsuzaki A, Bender MB. Eletrooculographic syndrome in monkeys after pontine reticular formation lesions. | Arch Neurol 1968;18:78-92. | 9. Fisher CM. Some neuro-ophthalmological observations. J. Neurol Neurosurg Psychiatry 1967;30:383-392. | 10. Goebel HH, Komatsuzaki A, Bender MB, Cohen B. Le- sions of the pontine tegmentum and conjugate gaze paralysis.
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